8917 RESULTS
COMMENT Though we have made substantial progress in characterizing the behavior of biochemical and imaging biomarkers in presymptomatic and manifest Alzheimer’s disease, we still need an inexpensive and noninvasive index for the presence of AD pathology and its ...
COMMENT This study involved persons with dominantly inherited Alzheimer disease mutations who donated plasma samples. The key finding was that ptau181 levels were elevated in both symptomatic and asymptomatic individuals and, in particular, modeling indicated ...
COMMENT This paper provides further evidence that plasma ptau181 may be an excellent blood-based biomarker for Alzheimer disease brain pathology and symptomatic status. Interestingly, the investigators found very high intra-individual variation in p-tau181 levels ...
COMMENT The paper describes changes in plasma concentrations of P-tau181 in familial Alzheimer’s disease. The authors found that similar to plasma NfL, the P-tau181 concentrations started to increase around 15 years prior to symptom onset. The unadjusted ...
COMMENT In this study of P-tau181 and NfL in plasma of familial Alzheimer’s disease, O’Connor et al. leverage an in-house-developed P-tau181 assay and commercial Quanterix NF-Light assay. This NfL assay is widely used. The P-tau181 assay, although new, is gaining ...
COMMENT In this study, Pandey et al. report that a γ marker (GM) allotype more susceptible to HSV-1 immune evasion mechanisms is present at higher rates in subjects with Alzheimer’s disease. The authors show that carriers homozygous for the GM 17 allotype were ...
COMMENT The paper by Palmqvist et al. on blood plasma phospho-tau 217 is a remarkable clinical study clearly demonstrating the value of phospho-tau 217 for identifying AD pathology. These findings advance our understanding of how p-tau217 is related to amyloid ...
COMMENT This unique paper deserves a broad readership because of the clever strategies the authors used in determining the role of inhibition of the complement system (via SRPX2) in regulating C1q activity, C3 levels and, in turn, preventing synaptic elimination ...
COMMENT This paper describes a novel complement inhibitor, SRPX2, expressed by neurons, that directly binds C1q and suppresses complement activation, C3 deposition on synapses, and subsequent C3-mediated synaptic elimination. They used CRISPR technology to ...
COMMENT I find the case made by Kim et al. to be convincing. Mutation detection is a difficult job. Usually, mutations are extremely rare and, as a result, difficult to find. My lab, as well as the labs of my mentors, Jason Bielas at the Fred Hutchinson Cancer ...
COMMENT Based on a reanalysis of the raw data published by Lee et al., 2018, a recent study by Kim et al. raised several concerns, including contamination of the sequencing library by a recombinant vector carrying an insert of APP. In their rebuttal, Lee et al. ...
COMMENT This elegant study extends the previous notion that neurodegenerative disorders are preceded by a long, clinically silent phase of at least several decades that might perhaps even start very early in life. Unsurprisingly, several aspects of mHTT mirror ...
COMMENT This is an interesting paper. In other single-gene neurodegenerative diseases, from prion to Alzheimer’s, there have been suggestions of potential neurodevelopmental influences, but this study takes an interesting approach to addressing this through the ...
COMMENT These data are very interesting. There has been debate in the Huntington’s disease field regarding the existence of a neurodevelopmental deficit. Evidence is accruing that this may be the case based on differentiating HD IPSc systems, mouse development, ...
COMMENT Excellent work by Tony Wyss-Coray's laboratory. It advances the field with impressive and exciting observations and hypotheses that confirm what several of our BBB colleagues have been discussing in recent years. I agree with Axel Montagne that this ...
